Monoclonal IgE with renal failure

Only four cases of immunoglobulin E (IgE) monoclonal “gammapathies”¹ have been reported previously. Discussed here is a 57 year old man who presented with hypertension and the nephrotic syndrome. A monoclonal IgE-kappa component (0.6 mg/ml), which did not appear as an M spike on protein electrophoresis, was demonstrated by immunoelectrophoresis in the serum and urine. The patient's condition deteriorated rapidly due to renal failure, and he died five weeks after the diagnosis was made. Pathologic examination disclosed extensive glomerular lesions, but amyloid was not detected by light or electron microscopy. The possible relationship between the monoclonal gammapathy and kidney impairment is discussed.     

Suppressive therapy of nontoxic goiter

In a double-blind study, 114 patients with clinically benign nontoxic goiter were treated either with liothyronine (T3), 50 μg/day, or thyroxine (T4), 200 μg/day. After 12 weeks of therapy, patients whose goiters decreased in size were continued on the same therapy for an additional 16 weeks. Those who did not respond were randomly divided into two groups: in one group the same dose of the same medication was continued, and in the other twice the dose of their original medication was given. By the end of 28 weeks, 40 of 54 patients treated with T3 and 29 of 59 patients treated with T4 showed a significant decrease in goiter size. The difference in effectiveness of the two agents was statistically significant (p < 0.025). Both T3 and T4 were effective in reducing small goiters, but T4 was relatively ineffective in shrinking large goiters. Duration of treatment, rather than dose of thyroid hormone, was the major determinant of goiter shrinkage.T3 produced a uniform and consistent depression of radioiodine uptake and circulating hormonal iodine levels, and was effective shrinking both small and large thyroid nodules, whether or not radioiodine uptake was reduced to hypothyroid levels. T4 uniformly increased circulating hormonal iodine levels. However, in T4-treated patients who responded with regression of thyroid nodules, suppression of radioiodine uptake was substantially greater than in those who did not respond.     

Bicarbonate and the regulation of ventilation

The regulation of ventilation involves a multifactorial control system with several feedback loops transmitting deviations from normal in pH, carbon dioxide tension (pCO₂) and oxygen tension (pO₂) to the control area. Variations in the size of the bicarbonate pool, caused by ventilatory or metabolic disturbances, can be expected to modify resting ventilation if hydrogen ion activity is the ultimate stimulus of the regulation of ventilation. A relationship between serum bicarbonate and resting ventilation can be identified in patients with stable acid-base disturbances including those in whom correction of the arterial blood pH was not achieved by respiratory adaptation. Why the pH in arterial blood is rarely returned to the normal range is not well understood. It may be an inadequacy of the control system, a “compromise” solution avoiding hypoxia in metabolic alkalosis or increasing work of breathing in metabolic acidosis, or a consequence of discrepancies in hydrogen ion activity in body fluids adjacent to and remote from the control site.Additional information about the role of bicarbonate in the control of ventilation may be obtained by measuring the response to carbon dioxide inhalation at varying extracellular bicarbonate concentrations. The increments in ventilation during inhalation of carbon dioxide are within individual limitations, inversely and exponentially related to the bicarbonate concentrations in blood.These observations are in accord with the concept that the extracellular bicarbonate concentration modulates resting ventilation and the ventilatory response to inhalation of fixed concentrations of carbon dioxide by acting as a determinant for the hydrogen ion activity within or adjacent to the central chemosensitive control area.     

Methyldopa hepatitis: A report of six cases and review of the literature

Six cases of methyldopa hepatitis, including two in which the patients died are reported; and 77 cases from the literature are reviewed. Patients in whom severe hepatotoxic reactions to methyldopa develop usually complain of prodromal symptoms typical of hepatitis, often with fever, one to four weeks after therapy is initiated. Jaundice, when it occurs, is usually manifest within three months.

Asymptomatic, transient elevations of serum transaminase levels may occur in patients receiving methyldopa. However, since the clinical and histologic features of hepatic injury from methyldopa are indistinguishable from viral hepatitis, it is suggested that the incidence of this iatrogenic disease is higher than generally appreciated.

Serum transaminase levels should be determined at the initiation of therapy with methyldopa and four weeks later. Moreover, any patient who has unexplained fever or the prodromal symptoms of hepatitis should undergo liver chemistry studies immediately.